Tachycardia Flashcards
people that present with tachycardia and heart palpitations should get what test
12 lead EKG
what is narrow complex tachycardia
- sinus tachycardia
- AV nodal re-entrant tachycardia
- AV reciprocating tachyc ardia orthodromic
- multifocal atrial tachy
- atrial fibrillation
- atrial flutter
what is wide complex tachycardia
- AVRT - antidromic - WPW
- ventricular tachycardia
- ventricular fibrillation
etiologies of sinus tachy
- exercise
- ansxiety
- pain
- exposure to stimulants (caffeine)
- volume depletion (dehydration/sepsis)
- anemia
- hypoxia
- hyperthyroidism
- pulm embolism
- pericarditis
symptoms of sinus tachy
asymptomatic
heart palpitations
SOB (esp with exertion)
symptoms of sinus tachy in pts with heart dz
heart palpitations SOB chest discomfort lightheadedness fatigue
treatment of sinus tachycardia
treat underlying cause:
- dehydration - IV fluid
- pain - pain meds
- pulm embolism - anticoagulants
- sepsis - treat source
- anxiety - consider anxiolytics
**No specific treatment for the tachycardia itself
what is supraventricular tachycardia
- regular, rapid rhythm
- narrow complex (originates above ventricles)
- no discernible p waves
examples of supraventricular tachycardia
atrioventricular nodal reentry tachycardia
orthodromic AV reciprocating tachycardia
junctional tachycardia
symptoms of SVT
- sudden onset racing heart palpitations
- lightheadedness, pre syncope, syncope
- SOB
- anxiety
- if underlying heart dz: chest pain
- often self limiting, ends abruptly as well
begins suddenly and ends suddenly
management of persistent SVT stable pts:
- vagal maneuvers
- carotid massage (listen for bruit, risk of stroke esp >50yo)
- adenosine (initial dose 6mg IVP, then 12mg IVP, then 12mg IVP)
- CCB or BB
tx for pts with frequent attacks of SVT
consult EP –> confirm aberrant pathway –> radiofrequency catheter ablation
management of persistent SVT unstable pts:
vagal maneuvers then if unsuccessful immediate DC cardioconversion
what is DC & how does it work
direct cardioconversion
- medical procedure which converts cardiac arrhythmias to normal sinus rhythm using electricity
- two electrode pads are placed on the pt (chest and back)
- electrode pads are connected to a machine via cables
- the cardioverter delivers a shock which causes momentary depolarization of most cardiac cells allowing the sinus node to resume normal pacemaker activity
what is (AVNRT)
- which gender more predominant
- triggered by?
- HR
atrioventricular nodal reentrant tachycardia
- most common cause of SVT
- 75% female
- reentrant circuit around the AV node
- healthy hearts and sick hearts
- triggered by exertion, caffeine, alcohol
- HR 140-280 regular
what is AVRT
atriventricular reciprocating tacycardia
- accessory pathway
- healthy and sick hearts
- wide or narrow QRS complexes
- seen in WPW
tx of stable pts with narrow complex (orthodromic) AVRT
- vagal maneuvers
- adenosine
- CCB or BB
if orthodromic AVRT is associated with afib/flutter how would you treat?
avoid nodal blocking meds, use class Ia, Ic II antiarrhythmics - procainamide
how would you treat orthodromic AVRT in unstable pts
immediate cardioversion
orthodromic AVRT
antidromic AVRT
- orthodromic = narrow complex
- antidromic = wide complex
antidromic AVRT is difficult to distinguish from what?
ventricular tachycardia
immediate tx of antidromic AVRT: unstable vs stable if you know it’s a preexcitation syndrome
immediate DC in unstable pts
procainamide in stalbe pts
subsequent tx of antidromic AVRT
catheter radiofrequncy ablation of accessory pathway
what is WPW
-pre-excitation syndrome involving an accessory pathway
how many pts are symptomatic in WPW
25-50%
range of symptoms in WPW
palpitations to syncope
most common cause of WPW on EKG
paroxysmal supraventricular tachycardia which is usually AVRT
distribution of people affected by WPW
bi modal
- early childhood
- early adulthood
1/3 of pts with WPW also have
afib - potentially serious arrhythmia in WPW pts
- afib may result in rapid ventricular response
- subsequent degeneration to ventricular fib = sudden death
management of WPW with normal rate and stable
- catheter ablation of accessory pathway (standard of care)
- medical therapy if unable (BB, adenosine, antiarrhythmics - procainamide, amiodarone)
management of WPW with fast rate
same as other forms of AVRT
- unstable: DC
- stable: procainamide
- subsequent: catheter radiofrequency ablation
what is multifocal atrial tachycardia
-therapy?
>=3 p wave morphologies 100-150bpm -therapy involves tx of underlying medical problems (typically pulm dz) -verapamil -flecainide or propafenone
what is ventricular tachycardia (sustained)
- associated with what?
- rate?
- complication of what conditions?
-fast wide complex rhythm
-often associated with structural heart dz
-frequently associated with syncope
>= consecutive ventricular premature beats
-usual rate 160-240bpm
-moderately regular
-frequent complication of MI and dilated cardiomyopathy
symptoms of ventricular tachycardia
- asymptomatic
- heart palpitation
- lightheadedness
- chest pain
- SOB
- diaphoresis
- near syncope
- syncope
- sustained LOC
- pulseless electrical activity (death)
tx of acute ventricular tachycardia - pulse present
pulse present:
- if vtach causes hypotension, heart failure, myocardial ischemia = DC
- if pt is stable = amiodarone 150mg IV bolus followed by continuous infusion
- implantable cardioverter-defibrillator
tx of acute ventricular tachycardia - pulseless
- CPR
- DC
- epinephrine
what is NSVT
3+ consecutive ventricular beats
- a rate of >120 bpm
- duration of less than 30s
NSVT
- symptoms
- how is it found?
- prognosis in healthy vs structural heart dz
- potential marker for what?
- common
- asymptomatic
- dx on routine EKG or exercise stress test
- usually benign
- potential marker for development of sustained ventricular arrhythmias and sudden death
- in presence of structural heart dz, more serious pronogisis
goals of tx for NSVT
- prevent sustained arrhythmia and sudden death
- eliminate symptoms
NSVT and associated diseases
- hypertrophic cardiomyopathy - 25%
- idiopathic dilated cardiomyopathy - 80%
- valvular heart dz - 20% of pts with MVP, MR, AS
- chorinc coronary heart dz
- left ventricular dysfunction
management of NSVT
-frequent vs infrequent
- if infrequent, no specific intervention except:
- optimize electrolytes, BB, manage underlying conditions/risk modification - frequent: consider amiodarone
what is torsades de pointes
a type of vtach
what is torsades de pointes triggered by
hypokalemia, hypomagnesemia, drugs that prolong QTc
meds that prolong QTc - antiarrhythmic agents
antiarrhythmic agents:
amiodarone
flecainide
sotalol
meds that prolong QTc - antipsychotics
chlorpromazine haloperidol olanzapine quetipine risperidone
meds that prolong QTc - antibiotics
macrolides (azithro)
quinolones (levo/cipro)
meds that prolong QTc - antidepressants
citalopram
tricyclic antidepressants
tx of torsades de pointe
unstable - prompt defibrillation
stable - IV magnesium (1st line); temp transvenous overdrive pacing if no response to magnesium
ventricular fibrillation
often associated with severe CAD and caused by acute MI (ACS)
- sudden death may be initial manifestation of coronary dz in 20% of pts
- pts are pulseless and unresponsive
causes of ventricular fibrillation
- myocardial ischemia and infarction
- heart failure
- hypoxemia or hypercapnia
- hypotension/shock
- electrolyte imbalances
- stimulants (drugs, caffeine)
- preceded by Vtach
associated conditions with V fib
- LVH
- HOCM (hypertrophic obstructive cadriomyopathy)
- CHF
- AS
- brugada syndrome
tx of v fib
- cpr
- defibrillation
- if pulse regained = coronary arteriogrphy , (cardiac cath) to view and tx AAD
- implantalbe cardioverter-defibrillator
